| Identification | Back Directory | [Name]
AA9 | [CAS]
1467047-25-1 | [Synonyms]
SRS11-92
Benzoic acid, 4-(cyclohexylamino)-3-[(phenylmethyl)amino]-, ethyl ester
HT-1080,FRDA,Friedreich,Inhibitor,cell death,ataxia,SRS-11-92,SRS1192,Ferroptosis,inhibit,SRS11 92,SRS11-92 | [Molecular Formula]
C22H28N2O2 | [MDL Number]
MFCD32867319 | [MOL File]
1467047-25-1.mol | [Molecular Weight]
352.47 |
| Chemical Properties | Back Directory | [Boiling point ]
523.7±45.0 °C(Predicted) | [density ]
1.152±0.06 g/cm3(Predicted) | [storage temp. ]
4°C, protect from light | [solubility ]
DMF: 30 mg/ml; DMF:PBS (pH 7.2) (1:4): 0.2 mg/ml; DMSO: 10 mg/ml; Ethanol: 10 mg/ml | [form ]
A crystalline solid | [pka]
5.48±0.20(Predicted) | [color ]
White to off-white |
| Hazard Information | Back Directory | [Uses]
SRS11-92, a Ferrostatin-1 (Fer-1) analogue, is a potent ferroptosis inhibitor. SRS11-92 inhibits ferroptotic cell death induced by Erastin in HT-1080 human fibrosarcoma cells (EC50=6 nM)[1]. | [Definition]
ChEBI: SRS11-92 is an ethyl ester resulting from the formal condensation of the carboxy group of 3-(benzylamino)-4-(cyclohexylamino)benzoic acid with ethanol. It is a potent inhibitor of ferroptosis induced by erastin in HT-1080 human fibrosarcoma cells (EC50 = 6 nM). It has a role as a ferroptosis inhibitor. It is a substituted aniline, an ethyl ester, a secondary amino compound and a diamine. It is functionally related to a ferrostatin-1. | [Biological Activity]
SRS11-92 is a cell penetrant and potent inhibitor of ferroptosis th at attenuates the cell death associated with frataxin knockdown in healthy human fibroblasts. SRS11-92 protects against cell death in in a brain slice model of Huntington′s diseasean oligodendrocyte model of periventricular leukomalaciaand in isolated kidney proximal tubules model of kidney disfunction. | [in vivo]
SRS11-92, used at 500 nM, is efficacious in protecting human and mouse cellular models of Friedreich ataxia (FRDA) treated with ferric ammonium citrate (FAC) and an inhibitor of glutathione synthesis (BSO), whereas caspase-3 inhibitors fail to show significant biological activity[2]. | [References]
[1] Skouta R, et al. Ferrostatins inhibit oxidative lipid damage and cell death in diverse disease models. J Am Chem Soc. 2014;136(12):4551-4556. DOI:10.1021/ja411006a
[2] Cotticelli MG, et al. Ferroptosis as a Novel Therapeutic Target for Friedreich's Ataxia. J Pharmacol Exp Ther. 2019;369(1):47-54. DOI:10.1124/jpet.118.252759 |
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